Short stature has been identified as a risk factor for gestational diabetes mellitus (GDM), although the pathophysiological basis for this association is not clear (1–3). In this context, we sought to evaluate the relationship between height and parameters of glucose homeostasis, including insulin sensitivity and β-cell function, in 671 Caucasian women undergoing a 3 h 100-g oral glucose tolerance test (OGTT) in late pregnancy. As previously described (4), the OGTT stratified subjects into three groups: GDM (n = 126), gestational impaired glucose tolerance (GIGT) (n = 117), and normal glucose tolerance (NGT) (n = 428). Insulin sensitivity and β-cell function were assessed by the insulin sensitivity index for OGTT (ISOGTT) and the Insulin Secretion-Sensitivity Index-2 (ISSI-2), respectively.

This study confirms the independent negative association between height and postchallenge glycemia previously observed in other ethnically-homogeneous populations (1–3). Importantly, however, we extend this literature by showing that these relationships remain significant after adjustment for GDM and, in fact, are present in the normoglycemic range. This observation potentially supports the notion of an underlying biological basis and underscores the need to examine the relevant pathophysiology. In this context, however, our multiple linear regression analyses suggest that neither insulin sensitivity nor β-cell function account for the relationship between height and postchallenge glycemia. The possibility of an artifactual basis for this relationship (wherein the standardized 100-g glucose load represents a greater glycemic stimulus in shorter women than in their taller peers) has been debated in the literature (1,5). At present, we can only postulate that short stature may be a modest marker or epiphenomenon identifying women at risk of GDM, with the underlying biology still unclear.

Our study is limited by the absence of assessment of leg length, which Moses and Mackay (2) have previously shown to be the precise anthropometric measurement that relates height to glycemia. In addition, we did not assess diet and socio-economic status, which are potential confounding factors. Further study will be needed to address the basis for the inverse relationship between stature and postchallenge glycemia in pregnancy.

Acknowledgments

This study was supported by operating grants MOP 67063 and 84206 from the Canadian Institutes of Health Research (CIHR), OG-3-08-2543-RR from the Canadian Diabetes Association (CDA), and NA 6747 from the Heart and Stroke Foundation of Ontario (HSFO). R.R. holds a CIHR New Investigator Award and has received CDA Clinician-Scientist incentive funding and University of Toronto Banting and Best Diabetes Centre New Investigator funding. A.J.H. holds a Tier-II Canada Research Chair in Diabetes Epidemiology. B.Z. holds the Sam and Judy Pencer Family Chair in Diabetes Research at Mount Sinai Hospital and University of Toronto.

No potential conflicts of interest relevant to this article were reported.